Rebecca Walker Short Biography Essay Example for Free

Rebecca Walker Short Biography Essay Rebecca Walker is a writer, philanthropist, feminist, and mother. She is the daughter of Alice Walker, who was also a famous feminist and writer. Growing up with a mother who was an active radical feminist heavily influenced her ideologies, although she states in her autobiography that she disagrees with many of Alice Walker’s more radical views. She has worked as a consultant on cultural diversity and gender roles for businesses like Sony, Microsoft, and JP Morgan. Rebecca Walker was born November 17, 1969 in Jackson Mississippi to Alice Walker and her husband Mel Leventhal, and Jewish American Lawyer. Her parents divorced when she was eight and she spent her childhood moving back and forth between her mothers home in San Francisco in a predominantly African American neighborhood and her Fathers home in New York in a Jewish neighborhood. While Walker was staying in San Francisco, she spent most of her time being looked after by relatives or neighbors because her mother was frequently away working in the feminist movement. Walker had the drive and determination to be able to receive an excellent education. She was able to receive an education at a private high school, the Urban School of San Francisco. She graduated from Yale University in 1992. In the same year, she helped found the Third Wave Foundation, a women’s leadership and activism organization. During her career as a writer, Walker has written in the subjects of gender roles, racism, sexism, politics, sexual orientation, and third wave feminism. In her autobiography Black, White, and Jewish: Autobiography of a Shifting Self she speaks about her parents’ divorce and how her bisexuality, and her biracial and bicultural heritage has affected her life. Walker had also been a contributor to several magazines and other publications. In her book To Be Real: Telling the Truth and Changing the Face of Feminism, Walker talks about her feminist views and call out her mother’s generation of feminists for â€Å"for denigrating men and encouraging women to seek independence whatever the cost to their families. † (Walker 1995). Walker became an active member of the feminist movement in 1992 shortly after she graduated from Yale. She helped co found the Third Wave Foundation Walker speaks at universities and conferences about multiculturalism, equality, intergenerational cooperation, and third–wave feminism. Walker says that the goal of third-wave feminism should not be to raise women above men, as she said her mother believed should be done, but to seek true equality for all people. Her books explained that feminists also need to work towards equality for other people in need like victims of racial discrimination and those living in poverty. As an adult, Rebecca Walker became estranged from her mother. The two frequently disagreed over Rebecca’s ideologies, which were not as radical as her mother’s. In 2004, Rebecca and her partner Choyin Rangdrol, a Buddhist teacher, had their first son Tenzin when Rebecca was thirty five years old. In 2007, Walker published her book Baby Love: Choosing Motherhood After a Lifetime of Ambivalence. Walker encourages feminists to pay attention to their age and not to miss out on the opportunity to be a mother and states the fact that she regrets waiting so long herself, as she is now unable to have second child. She argues against radical feminist ideas that motherhood is a burden to women and instead calls it a blessing. Walker has received many awards for her writing and for her activism work. She has received the â€Å"Feminist of the Year† award, the â€Å"Woman of Distinction† award, and the â€Å"Women Who Could be President† award. Her autobiography Black, White, and Jewish: Autobiography of a Shifting Self was given the Alex Award by the American Library Association.

Serum Urate Concentrations and the Risk of Hyperuricemia

Serum Urate Concentrations and the Risk of Hyperuricemia Common UCP2 variants contribute to serum urate concentrations and the risk of hyperuricemia Luyu Yang, Zheng Dong, Jingru zhou, Yanyun Ma, Weilin Pu, Dongbao Zhao, Hongjun He, Hengdong Ji, Yajun Yang, Xiaofeng Wang, Xia Xu, Yafei Pang, Hejian Zou,  Li Jin,  Chengde Yang*, Jiucun Wang* *Corresponding author These authors equally contributed to this study.   Abstract Elevated serum urate, which is regulated at multiple levels including genetic variants, is a risk factor for gout and other metabolic diseases. This study aimed to investigate the association between UCP2 variants and serum urate as well as hyperuricemia in a Chinese population. In total, 4332 individuals were genotyped for two common UCP2 variants, -866G/A and Ala55Val. These loci were not associated either serum urate level or with a risk of hyperuricemia in the total group of subjects. However, in females, -866G/A and Ala55Val were associated with a lower serum urate (P = 0.006 and 0.014à ¯Ã‚ ¼Ã…’seperately) and played a protective role against hyperuricemia (OR = 0.80, P = 0.018; OR = 0.79, P = 0.016). These associations were not observed in the males. After further stratification, the two loci were associated with serum urate in overweight, but not underweight females. The haplotype A-T (-866G/A-Ala55Val) was a protective factor for hyperuricemia in the female subgroup (OR = 0.80, P=0.017). This present study identified a novel gene, UCP2, that influences the serum urate concentration and the risk of hyperuricemia, and the degree of association varies with gender and BMI levels.   Introduction Uric acid is the final product of purine oxidation in humans. Elevated serum urate, or hyperuricemia, has long been recognized as an independent risk factor for gout [1-2]. There is a renewed interest in hyperuricemia and its association with a number of other clinical disorders including hypertension, atherosclerosis, cardiovascular disease, chronic kidney diseases, and abdominal obesity, glucose intolerance, insulin resistance, and dyslipidemia, which are often subsumed under the term metabolic syndrome [3]. Serum urate is balanced between uric acid production in the liver and its disposal via the kidney and gut [4]. The occurrence of hyperuricemia could be caused by disruptions in any part of this metabolic process. Both genetic and environmental factors, such as gender and body mass index (BMI), have a strong effect on the risk of hyperuricemia [3]. Among those factors, the attribution of genetic factors is estimated to be as high as 73% [5]. Recent genome-wide association studies (GWAS) have identified 28 loci associated with serum urate concentration [6]. However, only approximately 7% of the variation in serum urate concentration could be explained by those reported loci, suggesting the missing heritability remained to be explored [6]. Human uncoupling proteins (UCPs) are mitochondrial transporters present in the inner membrane of mitochondria [7]. UCPs are capable of uncoupling ATP production from mitochondrial respiration by causing proton leak and preventing mitochondrial hyperpolarization and the formation of reactive oxygen species (ROS) [8]. Among the five identified UCPs, UCP2 is widely expressed in almost all mammalian tissues including white adipose tissue, liver, kidney, pancreatic islets, macrophages and retinal endothelial cells, indicating its involvement in a variety of physiologic or pathologic events [9-12]. Two of the most common polymorphisms of this gene, -866G/A (rs659366) in the promoter and Ala55Val (rs660339) in codon 55, were identified as being associated with different phenotypes [7, 12], including obesity, insulin resistance, type 2 diabetes mellitus (T2D), low-density lipoprotein (LDL) particle size, coronary incidence and other metabolic disorders [9-10, 13-21]. Given the involvement of UCP2 and hyperuricemia in a variety of metabolic disorders, we selected the two common loci -866G/A and Ala55Val to explore the association between genetic UCP2 variants and hyperuricemia in a Chinese population, offering a new diagnostic or therapeutic target for hyperuricemia. Results There was no  association between SNPs and serum urate The two loci were proven in Hardy-Weinberg equilibrium (-866G/A: P = 0.990; Ala55Val: P = 0.690). For -866G/A, AA, AG, and GG genotypes accounted for 21.6%, 49.9%, and 28.6% of hyperuricemic patients, respectively; in healthy controls, the distribution was 21.2%, 49.6%, and 29.3%, respectively. As shown in Table 1, the -866G/A polymorphism was not found to be associated with serum urate (AA/GG: Beta = -0.008, P = 0.644; AG/GG:Beta = -0.012, P = 0.474) or with the risk of hyperuricemia (AA/GG: OR = 1.05, P = 0.603; AG/GG:OR = 1.03, P = 0.667). For Ala55Val, the TT, TC, and CC genotype distribution was 21.5%, 50.5% and 28.0% in hyperuricemic patients, respectively, and the distribution was 21.5%, 49.8% and 28.6% in healthy controls, respectively. No association was observed between Ala55Val polymorphism and serum urate (TT/CC: Beta = -0.013, P = 0.460; TC/CC:Beta = -0.017, P = 0.324). There was no difference in the distribution of the genotypes or alleles among hyperuricemic patients a nd healthy controls (TT/CC: OR = 1.02, P = 0.824; TC/CC:OR = 1.04, P = 0.652). Therefore, no statistically solid evidence supported the genetic effect of -866G/A and Ala55Val on serum urate or the risk of hyperuricemia in the total group of subjects. UCP2 variants were associated withserum urate andhyperuricemia in female subgroups As shown in Table 1, we stratified all subjects into male and female subgroups to further explore the gender-related genetic effects of the two polymorphisms. In the male subgroups, there were no significant associations between the two loci and serum urate or the risk of hyperuricemia (all P > 0.025). However, some nominal significant associations were found between -866G/A and the hyperuricemia risk (genotype AA: OR = 1.26, P = 0.038; allele A: OR = 1.12, P = 0.035), indicating a possible risky effect of the -866G/A variant on hyperuricemia incidence in males. A significant association was found between SNPs and serum urate and hyperuricemia in the female subgroups. The -866G/A genotypes were associated with a lower serum urate (AA/GG: Beta = -0.078, P = 0.015; AG/GG: Beta = -0.104, P = 0.001) and a decreased risk of hyperuricemia (AG/GG: OR = 0.71, P = 0.025). The subjects carrying allele A had a lower serum urate and a decreased risk of hyperuricemia (A/G: Beta = -0.054, P = 0.006; OR = 0.80, P = 0.018). For Ala55Val, genotype TT carriers showed a lower serum urate (TT/CC: Beta = -0.075, P = 0.022) and a decreased risk of hyperuricemia (TT/CC: OR = 0.64, P = 0.020). Genotype TC carriers only had a lower serum urate (TC/CC: Beta = -0.082, P = 0.012) but no decreased risk of hyperuricemia (TC/CC: OR = 0.77, P = 0.093). Allele T was associated with a lower serum urate (T/C: Beta = -0.049, P = 0.016) and a decreased risk of hyperuricemia (T/C: OR = 0.79, P = 0.016). Further analysis of associationin females  with different BMI levels Further analysis was performed regarding the genetic effect of UCP2 variants on serum urate and the risk of hyperuricemia among females with different BMI levels (Table 2). The majority of the females enrolled were stratified into normal- or overweight group (Table 2). In the underweight subgroup, whose sample size was limited after stratification, no significant association was observed between the two loci and serum urate or hyperuricemia risk (all P > 0.025, Table 2). In the normal weight subgroup, -866G/A genotype AA+AG carriers were associated with a lower serum urate (AA+AG/GG: Beta = -0.095, P = 0.022) but not with a decreased risk of hyperuricemia (AA+AG/GG: OR = 0.65, P = 0.076). However, the Ala55Val genotypes or alleles showed no statistical association with serum urate (TT+TC/CC: Beta = -0.070, P = 0.091; T/C: Beta = -0.047, P = 0.106) or hyperuricemia (TT+TC/CC: OR = 0.72, P = 0.173; T/C: OR = 0.72, P = 0.051). In the overweight subgroup, the genotypes of both loci were associated a lower serum urate (AA+AG/GG: Beta = -0.138, P = 0.001; TT+TC/CC: Beta = -0.130, P = 0.003) and a significant, or at least marginal, decreased risk of hyperuricemia (AA+AG/GG: OR = 0.62, P = 0.015; TT+TC/CC: OR = 0.74, P = 0.027). However, the alleles of the loci were associated with a lower serum urate level (A/G: Beta = -0.072, P = 0.019; T/C: Beta = -0.072, P = 0.019) but not with a decreased risk of hyperuricemia (A/G: OR = 0.75, P = 0.036; T/C: OR = 0.74, P = 0.027). Our results suggested a stronger effect of UCP2 variants on overweight females than on normal weight females (Table 2). Association between haplotypes and risk of hyperuricemia As listed in Table 3, the haplotypes of the two loci were estimated in the total group of subjects and after stratification by gender. The -866G/A and Ala55Val variants were in strong linkage disequilibrium (D = 0.974, r2 = 0.936). The wild type haplotype G-C (-866G/A-Ala55Val) was applied as the reference one. Haplotype A-T made up for the most frequent one, while single mutation at -866G/A or Ala55Val each accounted for less than 1 percent (Table 3). In the total group of subjects, no haplotypes were correlated with susceptibility of hyperuricemia. In the female subgroups, haplotype A-T (-866G/A-Ala55Val) was associated with a decreased risk of hyperuricemia; however, this association was null in males. No further significant associations between hyperuricemia and other two rare haplotypes were found in our study, partly due to the limited size of the rare haplotypes carriers (Table 3). These results correlated with the association between genotypes or alleles and hyperuricemia (Ta ble 1). Discussion Uncoupling protein 2 (UCP2) is present in the inner mitochondrial membrane and mainly decreases the ATP level and ROS produced by electron transport; therefore, UCP2 is involved in a board range of pathological processes. In the present study, we first focused on the relationship between UCP2 variants and serum urate and hyperuricemia, potentially examining the scope of the loci related to hyperuricemia. The present study revealed no association between the two polymorphisms of UCP2 and serum urate or hyperuricemia in the total group of subjects. However, because serum urate is extensively influenced by gender differences, we stratified the total group of subjects and determined that -866G/A and Ala55Val were associated with serum urate and hyperuricemia in females [25-26]. Females with the -866G/A genotype AA+AG or allele A had lower serum urate and a decreased risk of hyperuricemia, indicating a protective role of -866G/A for hyperuricemia in females. The -866G/A variant is a functional polymorphism located in the promoter region and putatively changes the transcription factor binding sites [7]. The wild type G allele in -866G/A was associated with lower UCP2 mRNA expression [19, 27]. Increased UCP2 mRNA expression from the A allele was translated into an increased amount of UCP2 protein, with corresponding induced proton leak, decreased ATP/ADP ratio and enhanced elimination of ROS [10, 19]. Hypermethylation in the promoter region could affect the binding of transcripation factors, causing aberrant gene expression. Consistent with our expectations, we found a typical CpG island in the UCP2 promoter region, which included the locus of the -866G/A variant, using information from the University of California-Santa Cruz (UCSC; Santa Cruz, CA, USA) database (http://genome.ucsc.edu/cgi-bin/hgGateway). We believe the UCP2 promoter variant -866G/A could shape this CpG island and protect the UCP2 promoter region from DNA methylation, unco vering a novel underlying mechanism that determines -866G/A increases UCP2 transcription. Uric acid accumulation is caused by the acceleration of ATP degradation to AMP, a precursor of uric acid, and UCP2 could decrease the ATP level and lower redundant AMP for uric acid formation [7, 28]. Moreover, an elevation of serum urate concentration occurs as a physiologic response to increased oxidative stress [31]. Because the ROS level could be down-regulated by UCP2, a counter-regulatory increase of serum urate as an antioxidant defense is less urgent. Therefore, the -866G/A variant in the promoter region might serve as a protective factor through a higher UCP2 mRNA level and increased translation of the UCP2 protein, which might regulate ROS and modify the ATP/ADP ratio. The other locus, Ala55Val, is a missense variant in exon 4 and is associated with an altered degree of uncoupling [7]. In our study, a protective effect for hyperuricemia and lower serum urate were observed in genotype TT and allele T in the female subgroups. However, the genetic effect of the Ala55Val variant was less clear. Several researchers identified an association of Ala55Val with the BMI level and type 2 diabetes mellitus (T2D), with controversial conclusions within cohorts, and few functional studies were performed [14, 32-33]. Similar to -866G/A, the protective role of the Ala55Val variant for hyperuricemia might also be attributed to altered UCP2 transcription. In the male subgroups, a less statistically significant but possible effect of -866G/A and Ala55Val was observed for hyperuricemia risk and higher serum urate. Similar gender-associated genetic effects of UCP2 variants were more or less observed for diseases other than hyperuricemia [7]. For example, Heidema et al. suggested a genetic effect of UCP2 on weight gain was regulated through different mechanism in males and females [34]. Lee, et al. demonstrated that the association between UCP2 variants and BMI was more apparent among female subjects [35]. Cheurfa et al. confirmed the association of UCP2 variants with coronary artery diseases in males but not females [36]. In the present study, we found UCP2 variants -866G/A and Ala55Val had a stronger effect on females with hyperuricemia. One possible explanation for the gender-associated genetic effects of UCP2 might be a regulation role of sex hormones such as estrogen. Estrogen was reported to repress UCP2 in a breast cancer cell line and papillary thyroid cancer cells [37-38]. Taken together, these results suggest the UCP2 protein level was down-regulated by estrogen in females but reversed by the variants of -866G/A and Ala55Val, providing a plausible explanation for the specific protective effects of UCP2 variants on females [37]. Genetic effects on hyperuricemia and obesity have been widely recognized [3]. In the present study, we found that -866G/A and Ala55Val were associated with lower serum urate and a decreased risk of hyperuricemia in overweight, but not underweight, females (Table 2). The relative small sample size might limit the correlation analysis in the underweight group. However, we did observe females with higher BMI level were more likely to benefit from the protective genetic effect of -866G/A and Ala55Val, where the association was significant between the two SNPs and serum urate level of risk of hyperuricemia. In the contrast, among the normal weight females, -866G/A, but not Ala55Val, showed a significant association with a low risk of hyperuricemia, indicating a less contribution from the protective effect of UCP2 variants than seen in overweight females. It was also implied from our results that the [tw1]functional à ¢Ã‹â€ Ã¢â‚¬â„¢866G>A promoter variant displayed a stronger effect. The interactions between obesity, uric acid and UCP2 were complicated. BMI has long been viewed as an essential factor influencing uric acid [3]. UCP2 transcription was activated by fatty acids [16]. A recent meta-analysis revealed that UCP2 -866G/A and Ala55Val are associated with a risk of obesity [32]. Subtle intermediary obesity related phenotypes such as elevated triglycerides, total cholesterol concentrations, increased the risk of dyslipidemia and circulating leptin levels were also observed to be correlated with UCP2 variants [40]. Based on these results, we assumed lipid metabolism material such as fatty acids participated in and enhanced the genetic effect of UCP2 variants on serum urate regulation, explaining the stronger genetic effect of UCP2 variants on females with higher BMI levels observed in the present study. The -866G/A and Ala55Val variants were in strong linkage disequilibrium (D = 0.974, r2 = 0.936). The haplotype frequency analysis revealed that variants of the two loci were more in co-variant haplotype A-T (-866G/A-Ala55Val) compared with the single variant forms of G-T or A-C (Table 3). Haplotype A-T was associated with a decreased risk of hyperuricemia only in females, which was consistent with the genotype or alleles results. However, the small size of the two rare haplotypes might limit the power of association analysis with hyperuricemia risk to a certain extent. The susceptibility of hyperuricemia in the two rare haplotype carriers required validation in a larger cohort. Conclusion The present study identified a novel gene, UCP2, with two loci, -866G/A and Ala55Val; this gene influenced the serum urate concentrations and the risk of hyperuricemia in females. The associations of those loci were affected by gender and BMI. This study supported the potential involvement of this gene in the prevention, prediction and treatment of hyperuricemia. Materials and methods Experimental design A total of 4332 subjects were enrolled from the Taizhou Longitudinal Study [22] and included 1387 hyperuricemic patients and 2945 healthy controls. The associations of common UCP2 variants with serum urate and hyperuricemia were tested by linear regression and logistic regression with or without gender stratification, respectively. A body mass index (BMI) subgroup was also used for further analysis. Participants All subjects were enrolled from Taizhou Longitudinal Study [22], of which 1387 individuals had serum urate level over 7 mg/dl and were treated as hyperuricemic patients, and 2945 individuals had normal serum urate (à ¢Ã¢â‚¬ °Ã‚ ¤ 7 mg/dl) and were treated as healthy controls [23]. The subjects were divided into subgroups (underweight: BMI à ¯Ã¢â€š ¬Ã‚ ¼ 18.5; normal weight: 18.50 à ¯Ã¢â‚¬Å¡Ã‚ £ BMI Genetic analysis Genetic analysis was carried out in accordance with the written informed consent and guideline offered by the Ethical Committees of the School of Life Science of Fudan University. For genetic analysis, peripheral blood was collected from all the individuals included in this study. Genomic DNA was extracted from whole blood using the QIAamp DNA Blood Mini kit (QIAGEN, Germany) and was stored at -20à ¢Ã¢â‚¬Å¾Ã†â€™. The DNA concentration and quality (including optical density (OD) 260/280 and 260/230 measurements) were determined using a Nanodrop Lite spectrophotometer (Thermo Fisher Scientific, Waltham, MA, USA). Genotyping of -866G/A and Ala55Val in UCP2 were performed by SNPscan according to the manufacturers instructions. Statistical analysis The clinical characteristics were presented as the mean à ¯Ã¢â‚¬Å¡Ã‚ ± SD. Students t-test was used to test for a significant difference in the mean age, BMI and serum urate between hyperuricemic patients and healthy controls. The chi-square test was used to describe the gender distribution difference between hyperuricemic patients and healthy controls. The chi-square test was used to test Hardy-Weinberg equilibrium (HWE) of the two loci. We conducted a logistic regression analysis to calculate adjusted odd ratio (OR) with 95% confidence interval (95% CI) and P-values to describe the distribution of -866G/A and Ala55Val adjusted for age and gender between hyperuricemic patients and healthy controls. A linear regression was performed to calculate Beta and P-values to estimate the effect on serum urate in different genotypes and alleles. Genotype GG, allele G of -866G/A and genotype CC, allele C of Ala55Val were used as references, respectively. Stratification into subgroups was performed on the basis of gender and different BMI values for further analysis. Haplotype frequencies between the hyperuricemic patients and controls were estimated by OR (95% CI) and chi-square test. The haplotype of the most frequent (-866G/A-Ala55Val, G-C) was used as the reference. A 2-sided P-value less than 0.025 was considered statistically significant after multiple correlation by Bonferroni method. The PHASE program (V2.1) was used for haplotype frequencies estimation, and SPSS 19.0 was used for the statistical analysis. References 1. Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med 2005;143(7):499-516. 2.  Weaver AL. Epidemiology of gout. Cleve Clin J Med 2008;75 Suppl 5:S9-12. 3.  Billiet L, Doaty S, Katz JD, Velasquez MT. Review of hyperuricemia as new marker for metabolic syndrome. ISRN Rheumatol 2014;2014:852954. 4.  Hediger MA, Johnson RJ, Miyazaki H, Endou H. Molecular physiology of urate transport. Physiology (Bethesda) 2005;20:125-33. 5.  Kolz M, Johnson T, Sanna S, Teumer A, Vitart V, Perola M, et al.. Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations. PLoS Genet 2009;5(6):e1000504. 6.  Kà ¶ttgen A, Albrecht E, Teumer A, Vitart V, Krumsiek J, Hundertmark C, et al.. Genome-wide association analyses identify 18 new loci associated with serum urate concentrations. 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Diabetes 2008;57(4):1063-8. 35.Nadal-Serrano M, Sastre-Serra J, Pons DG, Miro AM, Oliver J, Roca P. The ERalpha/ERbeta ratio determines oxidative stress in breast cancer cell lines in response to 17beta-estradiol. J Cell Biochem 2012;113(10):3178-85. 36.Hima S, Sreeja S. Regulatory role of estrogen-induced reactive oxygen species in the modulatory function of UCP 2 in papillary thyroid cancer cells. IUBMB Life 2015. 37.Hamada T, Kotani K, Fujiwara S, Sano Y, Domichi M, Tsuzaki K, et al.. The UCP2-866 A/A genotype is associated with low density lipoprotein particle sizes in the general population. Med Sci Monit 2008;14(3):CR107-11. Acknowledgements This research was supported by grants from the Science and Technology Committee of Shanghai Municipality (11DJ1400100), International ST Cooperation Program of China (2013DFA30870), Ministry of Science and Technology (2011BAI09B00), and Program for 2012 Outstanding Medical Academic Leader for Hejian Zou. The computations involved in this study were supported by Fudan University High-End Computing Center. Author contributions statement

My Shoes Writing Skills Writing Assignment English Language Essay

My Shoes Writing Skills Writing Assignment English Language Essay If only my shoes could talk†¦ What an amazing story they would tell! An adventure full of comedy, mystery, romance, murder (well maybe not murder haha), but all rolled up into one tale. Really, what else is with you through all of the important moments in your life? Shoes are such a simple accessory and often chosen as an afterthought when the perfect outfit is picked out. If you think about it though, they really are an integral part. I think of my shoes as a companion who listens without judgment. They are a friend who offers support and comfort but still offers me a pinch every once in awhile to bring me back to reality. I dont remember my first steps but I know my shoes were there with me. I can imagine my parents holding my hands preparing to release me into my first stage of independence. What a scary moment it must have been for all of us. As they released my little fingers, it was then that those tiny shoes kept me balanced. Sure there were trips and falls along the way, but my shoes and I quickly began to work together. We were soon skipping, jumping, and running together. My shoes always told the tale of what I had done that day. If inspected carefully, one could even see spatters of what I had eaten that day. Somehow, Mom always knew if I had been running through the garden again. My shoes were with me on the first day of school. As I walked up to the front door of the big building I shuffled my feet. Somehow the muffled sound of my brand new shoes against the pavement made the walk a little less scary. My shoes got to witness my very first art project. My little white sneakers were a beautiful collage of color when we were through. Who knew the paint would drip off the brush like that? My shoes could even tell the tale of the mean boy who splattered ketchup all over my new dress. I bet my shoes felt left out! What stories they could tell about running free on the play yard without a care in the world. If my shoes could talk, I bet they would tell all about the time I won the big recess race. When I was eight, my shoes were with me to experience my first big heartache. As my parent sat me down for a serious talk, I stared down at my shoes blankly. They talked about how they love me and everything would be fine. As I began to realize what they were telling me, I knew I hated the word divorce. I wondered why parents couldnt be like shoes. Shoes were a pair for life and were no good without the other. I wonder if my shoes would talk about what it felt like when my little tears rained down on them like a spring shower. My shoes were there to support me each time I walked through the doors to their separate houses. I suppose to make a good story; my shoes would have to talk about me as a teenager. I sure put on a lot of miles then. I wonder if they would divulge all the juicy details of my first date. When I was 15, I set out on a new adventure with a brand new pair of shoes that were carefully chosen just for that night. We went to a place called the Varsity in Downtown Atlanta. As we sat together eating our hotdogs, I glanced down at my shoes whenever there was a lull in the conversation. Strange I know, but it seemed like I always thought of something to say. It ended up being a magical evening with a wonderful man. I will let the shoes tell the details if they ever decide to talk. Perhaps my shoes would talk about how that first date eventually led to marriage. When I was 21, I took one of the most wonderful trips in a beautiful new pair of shoes. I chose the perfect pair to accompany me on the most incredible journey. They were able to balance my trembling body as I slowly made my way down the aisle. Only my shoes could tell you how I made it all the way to my future husband at the front of the building. The way he looked at me made me feel like the most beautiful woman in the world. As we stood up there hand in hand, reciting our vows, my shoes were there to witness the sacred promises we made to each other. I wonder if they would talk about how magical it was when we shared our first kiss as husband and wife. Would they talk about the way we seemed to float across the floor as we shared our first dance together? The promises we made to each other helped us through many tough times. Every time I see that particular pair of shoes in my closet, it brings back all the feelings and emotions of that day we made the promises to each other. My shoes could tell you how I am feeling at any given moment without even speaking. For example, if I pull out my favorite pair of strappy high-heeled sandals and put them on, it usually means I am in a flirty mood. If I pull on my supportive running shoes, perhaps they are telling you that I am in an active mood. My fuzzy slippers might tell you that I am feeling a little lazy. They also give tell-tale signs of the places I have been. A weekend stroll through the park always leaves bits of grass on the bottom of my shoes as evidence. My shoes have played a very important part in my life. They have witnessed all of the good and bad times in my life, and they will be there to witness many more. Through every situation they have offered their support and listening ear without judgment or blame. I think my shoes would have a great story to tell if they could talk, but I might be in a little trouble if they shared everything!

Acupuncture: Chinese Medicine Essay -- essays research papers

Acupuncture: Chinese Medicine As with all things we know little about there is quite a bit of mystery surrounding acupuncture. The part people see the most is a person with needles sticking out of their flesh. Understandably being wary of sharp pointed objects being wielded by a complete stranger, this is often an obstacle that needs to be over come. The best way to do this is by becoming educated about how acupuncture is performed, where it came from, what it does, some of the benefits vs. the problems, and the different views about it. Though out the many different texts on acupuncture you find there is room for interpretation on how to perform it, what to use, and even where the pressure is placed. One thing you will find in common among these texts is this, acupuncture works to varying degrees.   Ã‚  Ã‚  Ã‚  Ã‚  The earliest recordings of the use of acupuncture go back 2,000 years. In China it is widely expressed that it has been in use for 4,000 years. The origins go back as early as the Stone Age where abscesses were punctured by sharp stones or bone fragments. ( History ) When you experience pain it is an instinctive reaction to apply pressure to that location. Such as when you get a toothache. Also the body may experience pain where the infection is not localized. Your body naturally sends you warning signals that something is wrong. The Ancient Chinese utilized these warnings, and developed an intricate system of these points over time through observation. It is easy to infer that applying pressure to relive pain with your hands evolved into the use of needles instead.   Ã‚  Ã‚  Ã‚  Ã‚  Tortoise shells have been found and dated back to 1500 B.C. – during the Shang Dynasty - recording the use of acupuncture. The first actual written text acclaiming acupuncture is called Nei Ching Su Wen. It is written into two basic sections. The Su Wen, or easy questions and the Lung Shu, or hard questions. This book basically lays out all the different points, but it is mostly a book on concept and theory. The Nei Ching Su Wen lays the basic rules of philosophy and treaties on health. These philosophies branched form two mainstream religions that abounded during the Warring States period in Chinese history. The first is Confucianism. The teachings of this â€Å" religion â€Å" stress that the body is scared and are against dissection or surgery. T... ... You have no nasty side effect of drowsiness, or being groggy. The vomiting and stomach irritation are a thing of the past. This technique is especially being used and experimented with in China.   Ã‚  Ã‚  Ã‚  Ã‚  There is also another branch of acupuncture being explored. It involves pressure points specifically I the ear. These points are being found to be connected to all other organs of the body. Although there are arguments that acupuncture is purely suggestion, they can be proven wrong. Suggestion cannot allow for a human being to under surgery with pain. The discovery of endorphins shows that a chemical process is instigated through pressure points. There is a chemical increase of endorphins when acupuncture is performed. Research being funded in China by the United States, and other Western countries, are going to lead us to a great break through some day. The future looks bright, and everyday we learn more and more. Some day we may learn the secret of why acupuncture works for now we will have to accept that it does work and try to combine old and new philosophies to reach a greater understanding.   Ã‚  Ã‚  Ã‚  Ã‚     Ã‚  Ã‚  Ã‚  Ã‚  

Untying the Knot :: essays research papers

Human beings have an unquenchable thirst for knowledge and an urgent drive for understanding. The further we go on our quest for absolute truth and the deeper we plunge into the heart of the ultimate reality, the more profound our questions become. Could there be something more to this world of ours than that which meets the eye? Is there some elaborate design behind the infinite galaxies, stars, and planets, or are we simply at the mercy of a chaotic and unordered universe? What is it that has given rise to the mysterious and unexplainable phenomenon that we have labeled the cosmos? Throughout history, we have attempted to answer these perplexing and ineluctable questions through myths, religion, or science. Apparent in many of these explanations is the idea of a unity, the â€Å"One†, or a single entity that comprises all of reality. To some, it is God’s presence. To others it is the Tao or simply â€Å"that which is, and, in the case of modern physics, it is infini tesimally small strings, oscillating and vibrating, like the strings of a violin, that comprise the fabric of our universe and â€Å"rhythmically beat out the laws of the cosmos† (18).   Ã‚  Ã‚  Ã‚  Ã‚  String theory is a revolutionary way of explaining the complexity of the cosmos. It is the unified theory of physics that Einstein searched for but never found. It forces us to look at the world in which we live in a drastically different and beautiful way. String theory states that all aspects of our universe consist of infinitesimally small, vibrating loops of energy (14). Like Pythagoras’ idea of the â€Å"music of the spheres†, these universal strings vibrate and oscillate, producing different notes in a cosmic symphony. Strings are the most basic constituents of matter, â€Å"atoms† in the true sense of the word. According to physicists, string theory may hold the key to understanding the inner workings of the universe. As Brian Greene states in his book The Elegant Universe:   Ã‚  Ã‚  Ã‚  Ã‚   String theory has the potential to show that all of the wondrous happenings in the universe--from the frantic dance of subatomic quarks to the stately waltz of orbiting binary stars, from the primordial fireball of the big bang to the majestic swirl of heavenly galaxies--are reflections of one grand physical principle, one master equation (5). String theory is the first theory able to combine the undeniable, yet conflicting truths of Einstein’s general theory of relativity and the newly emerging field of quantum mechanics.

The Power of The Sea-Wolf Essay -- Sea-Wolf Essays

The Power of The Sea-Wolf Jack London’s novel, The Sea-Wolf, has many different interpretations. The story can be read as a combination of the naturalistic novel and the sentimental romance, both very popular around the turn of the century. London also brings into play literary naturalism, in which human beings are characterized as just another species in nature, subject to all of Her cosmic forces. The Sea-Wolf fits almost perfectly the archetypal pattern of an initiation story. Depth and interest are added to The Sea-Wolf by successfully integrating these three elements -- the combination of two popular genres, literary naturalism, and the initiation story. One of the characteristics common to most naturalistic novels is the theme of survival of the fittest. This novel is very much in concordance with this theory, set up by Charles Darwin and his theory of natural selection. Both Humphrey Van Weyden and Maud Brewster are individuals who have never known physical hardship. They are both people "of the books", and find themselves in a foreign environment when stranded on this boat with a "regular devil" (49), Wolf Larsen. Humphrey Van Weyden, after going through an "initiation process" to be discussed later, finds himself unable to remember clearly anything else. "It seems as though I have lived this life always. The world of books is very vague, more like a dream memory than an actuality. I surely have hunted and forayed and fought all the days of my life" ( 229). Humphrey makes an almost perfect allusion to Darwin's survival of the fittest idea when talking to Wolf Larsen, "You were once, and able to eat, as you were pleased to phrase i t; but there has been a diminishing, and I am now able to eat you" (249). Even Maud ... ...led Hump. Hump survives this so-called "ordeal" and makes it to third stage of the initiation process -- the return to the group. With the beginning of this stage the initiate is transformed. "Hump" becomes Mr. Van Weyden, as Wolf Larsen promotes him to first mate to replace Johansen. He is now accepted as part of the group and he, unlike Larsen, has good rapport with all the crew members. After this last stage is complete is when he gets up the courage to flee the Ghost and Larsen, and run away with Maud Brewster. The Sea-Wolf is one of the richest, and most interesting, novels ever written. Jack London has used a variety of literary techniques to bring his story to life. Through the combination of two popular genres of the time (naturalistic and romance), the use of the literary naturalism, and the story of an initiation, London brings the characters to life.

Netflix Case

Davor Ramesa k0956979 Netflix case Executive summary What is Netflix’s strategy in the on-line movie rental market? What are Netflix’s sources of competitive advantage? Identify the competences key to the success of Netflix’s strategy and explain why. Netflix was a late entrant to the movie rental market and it was a first mover in the on – line movie rental market. Netflix’s strategy in the movie rental market is differentiation from traditional movie rental stores. Instead of attracting customers to a retail location, Netflix offered home delivery of DVDs through the mail. Why only DVDs? In 1998, most available movies were in VHS cassette format but Netflix concentrated on using only DVDs because its marketing strategy was to develop cross promotional programs with the manufacturers and sellers of DVD players, providing a source of content for the customers. Also, there was no competition in that niche market and DVDs were small and light which made them perfect for mail delivery. Netflix had several sources of competitive advantage. For starters, Netflix’s website included a search engine that allowed customers to easily sort through its selection by title, actor, etc. Using these search engine customers could easily and quickly find a movie that they would like instead of looking on shelves of a retail store. Netflix was using the US Postal Service to deliver DVDs directly to a customer’s home. It was more convenient for customers. They used similar pricing to that offered by traditional video stores in the beginning but what gave them the competitive advantage was moving to a subscription prepaid service. And, soon afterwards they offered unlimited rentals to customers because they were targeting another group of customers – ones that wanted the convenience of watching a movie at any time and change them unlimited during a month. Netflix’s engineers developed a proprietary recommendation system. They have done so because mostly the new movies were being rented and they wanted to balance customers demand. How did this system work? Upon signing into a new account for the first time, customers took a survey to identify their favorite movie genres, as well as rate specific movie titles. This survey gave enough data to Netflix’s engineers to build a base and understand better customer’s preferences. Also, Netflix’s size and growth rate generated a positive †network effect† from its large customer – generated rating system. Because it had the largest collection of movie ratings in the world, customers recognized that they were more likely to have their tastes and preferences accurately reflected from Netflix’s site. The key to success in Netflix’s strategy was hiring Ted Sarandos as chief content office to manage content acquisition. He managed (due to his relationships) to negotiate direct revenue – sharing agreements with nearly all the majors studios. So Netflix was able to improve its relationships with its suppliers. The benefit was not just lower acquisition costs but the promotion of lesser known movies. So, customers had the benefit of large variety of movies. Also, using the proprietary recommendation system and the national inventory Netflix was able to replicate almost perfect inventory. This gave them a serious competitive advantage, since retail stores needed three or five times the copies of a movie to satisfy the same customer demand. Assess Netflix’s performance? Use multiple performance measures (strategic and financial). Table below shows (in 000$) Netflix’s performance using 2 financial ratios in year 1998 and 2006. (source : Netflix 2006 10-k) As we can see from the table, in year 1998 Netflix had poor performance. We can see that it was losing 16. 84 thousands of dollars to subscription (sales= revenue of subscription). Net profit margin was not any better a -18. 940$ . We can see that their operating profit margin was 0. 69 thousands of dollars and net profit margin was 0,04 thousand of dollars in 2006. Why was there such a change in profitability? Answer lies in the number of total subscribers which has grown from 107 000 in 1999 to 6 316 000 in 2006. (source: Netflix 2006 10-k). Number of subscribers was constantly growing since 1998 due to good strategy decisions like : proprietary recommendation system , hiring of Ted Sarandos and opening more distribution centers. All of these moves had one purpose: to add value to their product by increasing customer’s satisfaction. How does Netflix’s strategy compare to Blockbuster? Compare and contrast each’s value chain. Factors which determine the value of the product: Price – of the movie Delivery Time – how long do the customers wait for getting the movie Convenience – what actions do the customers have to do to get the movie Other factors(recommendation system, availability of new movies) Late fees Although prices of Netflix and Blockbuster for a single DVD rental are now the same (10$ per movie-source: http://reviews. cnet. com/4520-11445_7-6325775-1. html), Netflix had an additional value because it offered unlimited rental with the same pricing (an example: you pay monthly fee and you can exchange movies, so you can watch several different DVD†s for the price of one). If you want to rent a movie from a Blockbuster retail store, you can do it in a relatively short time (time you need to get to a retail store) as management proclaimed 10 minute drive for 70% of US population. Delivery time for Netflix is their disadvantage in comparison to Blockbuster, it takes a day or two. Convenience – Netflix has the advantage here since you can order movies from the comfort of your home by using the internet. Blockbuster doesn’t have a recommendation system like Netflix. It only has an employee that can recommend movies to a customer. Netflix has advantage here since it can recommend a movie accordingly to the taste of each customer. New movies are available pretty much the same for both companies. Late fees – in 2005. Blockubuster decided to abolish late fees which gave them an advantage over Netflix, increasing customer satisfaction but also gave them significant costs: 60 milion $ marketing + 600 million dollar of revenue loss. What challenges and opportunities does Netflix face? What are the major risks? Major challenge for Netflix’s online DVD rental business is VOD (video on demand). VOD offers additional value to the customer – no waiting period, since it uses streaming technology to provide customers a movie with no waiting period. This is also an opportunity for Netflix since it has the possibility to implement this new technology into its core business but there are several cons of doing so. First issue is that this feature would cannibalize the core business because Netflix would replace stream of positive cash flows with another. Also Netflix found no way to differentiate itself against competitors like MovieLink and Vongo. Another major risks or challenges for Netflix are cable and satellite providers which offer pay-per-view system, providing HD on demand. For now these services had two primary limitations: technology and content availability. Another major challenge is the entry of Blockbuster in the DVD online rental market. As a bigger company Blockbuster has the financial funds to attract more subscribers using heavy marketing. This entry directly enters Netflix’s niche market and now Netflix has to find a way to differentiate. For starters, what would be Netflix’s entry strategy to these new markets? It could ship the DVDs from USA but this option would have serious disadvantages like import tariffs, shipping costs, long delivery time which would lead to customer dissatisfaction and a very small market share with probably losses rather than profits. If Netflix would open a subsidiary in Europe it would not have problems like the latter but it would need investors since financing the whole subsidiary may present a problem for Netflix. Another issue is that Europe, as a difference to the US, is consisted of many small independent countries with their own laws and import tariffs so this could be a problem as well. Another problem is the customers preferences. If Netflix would try to ship movies from the US (which would also present shipping costs) the European customers might not like US movies that much. They might prefer European movies better. Another issue is that Netflix doesn’t have an established relationship with any European movie studio. So they would lose the competitive advantage that they have in the US. Another problem is the language barrier. In many countries like Germany, Italy, or Spain, movies are synchronized into their mother tongue. So customers might not be willing to rent these movies in the English language. Another issue is the competition in Europe which perhaps would be more competent than Netflix since they know better the customers needs, laws, and other issues mentioned already. Netflix as a company started with an emerging technology – DVD, then. Now the new technology is Blu- ray and as the VHS format was replaced by DVD there are good chances that Blu-ray will replace DVD format. Because Blu-ray technology gives a better resolution than a DVD customers might be willing to switch so Netflix should start to fill its inventory with blu-ray discs and maybe like they did in the past with VHS promote and rent only Blu-ray discs. The goal for Netflix’s is to find the best media (low cost, high quality) for watching a movie or even better – no media at all. Netflix’s, as I see it, biggest threat to DVD rental business is online video streaming. Why? With this technology customers have no waiting period and complete convenience. And these are very important factors when customers are making their decision about watching a movie. Decisive competence key for Netflix is the recommendation system and they should use it with online video streaming.